immune_responses_to_influenza_pneumococcosfandomcom-20200213-history
Epidemiology in Humans
Bacterial CI commonly occurs within the first 6 days of IV infection, presents similarly to IV infection occurring alone and is associated with an increased risk of death (CHERTOW; MEMOLI, 2013). * Disease is caused by SP that are primed to move to tissue sites with altered nutrient availability and to protect themselves from the nasopharyngeal microflora and host immune response (PETTIGREW et al., 2014). Prospective Data * SP was the most common cause of bacterial CI with IV and accounted for 40.8% and 16.6% of bacterial CIs during pandemic and seasonal periods, respectively (WANG et al., 2011). * Pneumonia increased substantially during the 2009 pandemic, especially during peak IV activity, suggesting a strong association between IV activity and pneumonia incidence during the pandemic period (SELF et al., 2014). * The majority of deaths in the 1918–1919 IV pandemic likely resulted directly from secondary bacterial pneumonia caused by common URT bacteria (MORENS; TAUBENBERGER; FAUCI, 2008). * The risk of SP acquisition increased following IV acute respiratory illness. IV and parainfluenza acute respiratory illnesses appeared to facilitate SP acquisition among young children (GRIJALVA et al., 2014). * Regular IV seasons were characterized by increased rates of SP bloodstream infections. IV outbreak was characterized by higher rates of SP bacteremia among children (TASHER et al., 2011). * Higher invasive SP pneumonia rates occurred during the peak pandemic month compared to nonpandemic periods. The peak’s magnitude was similar to that seen during seasonal IV epidemics (FLEMING-DUTRA et al., 2013). * Invasive SP pneumonia was associated with, IV and ≥5 days of hospitalization (WOLTER et al., 2014). * Patients with IV-associated community-acquired pneumonia were significantly older, had been vaccinated less often and had preceding antibacterial treatment less often (VON BAUM et al., 2011). * Patients with IV-associated community-acquired pneumonia 30-day mortality was low (4.4%) and not different to that of patients with pneumonia caused by bacterial (6.2%) or viral (other than IV) pathogens (4%) (VON BAUM et al., 2011). * Patients with IV plus a bacterial pathogen (mixed IV-associated pneumonia) had a higher mortality than those with pure IV-associated pneumonia (VON BAUM et al., 2011). * The study supports a strong but short-lived interaction between IV and SP, with IV infection increasing susceptibility to SP pneumonia (SHRESTHA et al., 2013). * The incidence of invasive pneumococcal disease was statistically higher than that observed in the same time period in 2008 and 2010, with some differences in the epidemiological data, showing a close relationship between SP and IV (PEDRO-BOTET et al., 2014). * CI occurred in 3.1% of children with complicated pneumonia and was associated with higher odds of intensive care unit admission and receipt of mechanical ventilation, vasoactive infusions, and blood product transfusions as well as higher costs and a longer hospital stay. Children with IV CI were less likely to require readmission, although there was a trend toward higher odds of mortality for patients with CI (WILLIAMS et al., 2011). * High SP colonization density was associated with respiratory virus CI and invasive SP pneumonia (WOLTER et al., 2014).